During the first two trimesters of development, the fetus heals skin wounds in a scarless manner, a process that occurs very rapidly and without inflammation. In contrast, skin beyond the third trimester of development through adulthood heals more slowly, includes a significant inflammatory phase, and results in the formation of a permanent scar. Although adult wound repair exhibits a robust period of angiogenesis, wound angiogenesis has not been well described in scarless fetal healing. Our preliminary data suggests reduced levels of angiogenesis in scarless fetal wounds. The proposed studies will examine the contribution of wound angiogenesis to scar formation in fetal and adult skin. We will characterize wound angiogenesis and the production pattern of the pro-angiogenic molecule vascular endothelial growth factor (VEGF) and its receptors in fetal wound repair. In addition, we will examine the effects of VEGF-induced angiogenesis on scar formation using murine models of scarless fetal healing and adult wound repair. A better understanding of the scarless healing process that occurs in fetal skin could lead to the identification of therapeutic targets used to enhance the outcome of postnatal repair. [unreadable] [unreadable]